CCR5 -Δ32 gene polymorphism is related to celiac disease and autoimmune thyroiditis coincidence in patients with type 1 diabetes

Słomiński, Bartosz; Ławrynowicz, Urszula; Myśliwska, Jolanta; Ryba-Stanisławowska, Monika; Skrzypkowska, Maria; Myśliwiec, Małgorzata; Brandt, Agnieszka

doi:10.1016/j.jdiacomp.2016.10.031

Cited by 8 publications

(7 citation statements)

References 23 publications

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“…The VDR polymorphism FokI is associated with both T1D and AITD in the Brazilian Hispanic population ( 105 ). The chemokine receptor type (CCR)5 - 32 bp deletion (Δ32) is associated with both diseases and with celiac disease in Poland ( 141 ). Finally, the signal transducer and activator of transcription (STAT)-4 is associated with both T1D and AITD in Korea ( 140 ), SESN3 with AITD in the Chinese Han population ( 139 ) and SLC26A4 is associated with AITD in the Tunisian population ( 138 ).…”

Section: The Genetic Linkmentioning

confidence: 99%

Type 1 Diabetes and Autoimmune Thyroid Disease—The Genetic Link

Frommer

Kahaly

2021

Front. Endocrinol.

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Type 1 diabetes (T1D) and autoimmune thyroid disease (AITD) are the most frequent chronic autoimmune diseases worldwide. Several autoimmune endocrine and non-endocrine disorders tend to occur together. T1D and AITD often cluster in individuals and families, seen in the formation of autoimmune polyendocrinopathy (AP). The close relationship between these two diseases is largely explained by sharing a common genetic background. The HLA antigens DQ2 (DQA1*0501-DQB1*0201) and DQ8 (DQA1*0301-DQB1*0302), tightly linked with DR3 and DR4, are the major common genetic predisposition. Moreover, functional single nucleotide polymorphisms (or rare variants) of various genes, such as the cytotoxic T-lymphocyte- associated antigen (CTLA4), the protein tyrosine phosphatase non-receptor type 22 (PTPN22), the interleukin-2 Receptor (IL2Ra), the Vitamin D receptor (VDR), and the tumor-necrosis-factor-α (TNF) that are involved in immune regulation have been identified to confer susceptibility to both T1D and AITD. Other genes including cluster of differentiation 40 (CD40), the forkhead box P3 (FOXP3), the MHC Class I Polypeptide-Related Sequence A (MICA), insulin variable number of tandem repeats (INS-VNTR), the C-Type Lectin Domain Containing 16A (CLEC16A), the Erb-B2 Receptor Tyrosine Kinase 3 (ERBB3) gene, the interferon-induced helicase C domain-containing protein 1 (IFIH1), and various cytokine genes are also under suspicion to increase susceptibility to T1D and AITD. Further, BTB domain and CNC homolog 2 (BACH2), C-C motif chemokine receptor 5 (CCR5), SH2B adaptor protein 3 (SH2B3), and Rac family small GTPase 2 (RAC2) are found to be associated with T1D and AITD by various independent genome wide association studies and overlap in our list, indicating a strong common genetic link for T1D and AITD. As several susceptibility genes and environmental factors contribute to the disease aetiology of both T1D and AITD and/or AP subtype III variant (T1D+AITD) simultaneously, all patients with T1D should be screened for AITD, and vice versa.

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Section: The Genetic Linkmentioning

confidence: 99%

Type 1 Diabetes and Autoimmune Thyroid Disease—The Genetic Link

Frommer

Kahaly

2021

Front. Endocrinol.

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“…In studies on T1D patients, however, multiple reports have stipulated a protective role for this polymorphism. 10,38,39,79,80…”

Section: Sh2b Adaptor Proteinmentioning

confidence: 99%

Juxtaposition of Coeliac Disease and Type 1 Diabetes; the Role of Shared Non-Human Leukocyte Antigen Loci

Shahramian

Shahnazi

Bazi

et al. 2018

Int J Basic Sci Med

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Although extensive studies have been performed to explore the role of various alleles within the human leukocyte antigen (HLA) in susceptibility to coeliac disease (CD) and type 1 diabetes (T1D), less attention has been dedicated to the role of shred non-HLA loci. In present report, we have provided a review on the role of genetic variants in seven shared non-HLA loci in determination the risk of either CD or T1D. The literature search was done on the Web of Knowledge, PubMed, and Scopus databases using keywords of polymorphism, coeliac disease, and type 1 diabetes. The literature published within 2000-2017 were recruited. Seven discussed shared loci between CD and T1D were those resided within cytotoxic T-lymphocyte associated protein 4 (CTL4), regulator of G protein signaling (RGS1), SH2B adaptor protein (SH2B3), T cell activation Rho GTPase activating protein (TAGAP), interleukin 18 receptor accessory protein (IL18RAP), protein tyrosine phosphatase, non-receptor type (PTPN2), and C-C motif chemokine receptor (CCR5). Interaction between polymorphisms of these genes seems to exert a substantial impact on determination the risk of CD and T1D in context of each other. Polymorphisms residing in these loci can exert synergistic or opposing effects toward either protection or predisposition to CD and T1D. The majority of these polymorphisms affect the function of cytokine signaling or T cell activating pathways. The net outcome deems to be delineated by a complex interaction between these adaptor arms, as well as the modulatory effects of other components of immune system, in particular HLA alleles.

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“…The rs333 polymorphism has been related to the pathogenesis of several conditions beyond viral diseases such as celiac disease [23] and breast cancer [24]. Regarding the results on the rs333 polymorphism in the CCR5 gene and IBD, periodontitis and SLE, the data showed contradictories, which a better evaluation is required.…”

Section: Introductionmentioning

confidence: 99%

Relationship between the rs333 Polymorphism in the CC Chemokine Receptor Type Five (CCR5) Gene and Immunological Disorders: Data from a Meta-Analysis

Silva

Basic²,

Leal

et al. 2021

Int. J. Stats. Med. Res.

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Introduction: Inflammatory Bowel Disease (IBD), periodontitis and Systemic Lupus Erythematous (SLE) are multifactorial diseases, one of the factors in the course of these diseases is the rs333 polymorphism in the CC chemokine receptor type five (CCR5) gene. However, the results remain contradictory. Therefore, we aimed to perform a meta-analysis evaluating the relation between this polymorphism and the aforementioned conditions. Material and Methods: A search in the literature was performed in diverse scientific and medical databases for studies published before June 22, 2020. The data were extracted from the studies and the statistical evaluation was performed by the calculations of statistical heterogeneity (I²), Odds Ratio (OR) with 95% of Confidence Intervals (CI) and publication bias. The values of P<0.05 were considered as significant for all calculations. Results: 19 articles with 21 case/control studies in 4,304 case patients and 3,492 controls were included. The meta-analysis showed a non-significant association among the rs333 polymorphism and IBD (OR = 1.05, 95% CI: 0.91-1.20, P = 0.51), periodontitis (OR = 0.86, 95% CI: 0.64-1.17, P = 0.34) or SLE (OR = 1.00, 95% CI: 0.56-1.80, P = 1.00) under the allelic model or for any other performed calculation. There were no obvious publication bias in the analyses. Conclusion: In conclusion, this current meta-analysis evidenced the non-significant relation among the rs333 polymorphism and the risk of IBD, periodontitis or SLE. Further studies are required to validate our data.

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CCR5 -Δ32 gene polymorphism is related to celiac disease and autoimmune thyroiditis coincidence in patients with type 1 diabetes

Cited by 8 publications

References 23 publications

Type 1 Diabetes and Autoimmune Thyroid Disease—The Genetic Link

Type 1 Diabetes and Autoimmune Thyroid Disease—The Genetic Link

Juxtaposition of Coeliac Disease and Type 1 Diabetes; the Role of Shared Non-Human Leukocyte Antigen Loci

Relationship between the rs333 Polymorphism in the CC Chemokine Receptor Type Five (CCR5) Gene and Immunological Disorders: Data from a Meta-Analysis

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